title: [Inhibition of cardiac hypertrophy by mitofusin 2 in neonatal rat cardiomyocytes].
abstract: OBJECTIVE
  To study the expression and function of Mitofusin 2 (Mfn2) in cultured neonatal rat cardiomyocytes during PE-induced hypertrophy.
  
  
  METHODS
  The hypertrophy neonatal rat cardiomyocytes model was induced by 0.01 mol/L PE. RT-PCR and Western blot were applied to assess Mfn2 mRNA expression and protein level respectively. Cultured neonatal rat cardiomyocytes were treated by PE after Ad GFP or Ad Mfn2 infection, the protein synthesis was determined by 3H-leucine incorporation assay.
  
  
  RESULTS
  PE led to ANF mRNA level (by approximately 1 fold, P < 0.01) elevation and cell surface area (by approximately 1 fold, P < 0.01) increasing. Mfn2 mRNA (by approximatelt 50%, P < 0.01) and protein (by approximately 50%, P < 0.01) decreased remarkably in PE treated cardiomyocytes compared with those in control group. Compared with cells infected by Ad GFP (1.72+/-0.12 vs 2.47+/-0.06, P < 0.05, cell area (1.530+/-0.008 vs 0.830+/-0.009, P <0.01) and protein synthesis (0.98+/-0.10 vs 2.47+/-0.06, P < 0.01) were also largely abrogated in neonatal rat cardiomyocytes infected by Ad Mfn2.
  
  
  CONCLUSIONS
  These results indicate that the expression of Mfn2 mRNA and Mfn2 protein decreased in PE-induced neonatal rat cardiomyocytes hypertrophy model. Overexpression of Mfn2 in cultured neonatal rat cardiomyocytes could attenuate the protein synthesis and cell surface area increase after PE treatment. Accordingly, Mfn2 is an important regulator in cardiomyocytes hypertrophy.
authors.affiliation: Institute of Vascular Medicine, Peking University Third Hospital, Beijing 100191, China. chlchen@pku.edu.cn
authors.forename: Chun-lei
authors.initials: CL
authors.lastname: Chen
authors.forename: Tao
authors.initials: T
authors.lastname: Shen
authors.forename: Ming
authors.initials: M
authors.lastname: Zheng
authors.forename: Yan-hong
authors.initials: YH
authors.lastname: Guo
authors.forename: Xiao-jun
authors.initials: XJ
authors.lastname: Zhu
authors.forename: Guang-hui
authors.initials: GH
authors.lastname: Chen
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology*; D002478:Cells, Cultured; D020558:GTP Phosphohydrolases; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D051379:Mice; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D010656:Phenylephrine; D014176:Protein Biosynthesis / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014162:Transfection
chemical_list: D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D010656:Phenylephrine; D020558:GTP Phosphohydrolases; C489710:Mfn2 protein, rat